Gum Disease Bacteria Linked to Onset of Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects a person’s joints and internal organs, causing pain and leading to disability. Rheumatoid arthritis is more common in older people, but there is also a high prevalence in young adults, adolescents and even children, and it affects women more frequently than men.

The results of a new study presented at the Annual European Congress of Rheumatology (EULAR 2018) suggest that bacteria linked to periodontitis may play a key role in the onset and development of rheumatoid arthritis.

“It has been shown that RA-associated antibodies, such as anti-citrullinated protein antibodies, are present well before any evidence of joint disease. This suggests they originate from a site outside of the joints,” said study author, Dr Kulveer Mankia, of the Leeds Institute of Rheumatic and Muscoskeletal Medicine.

“Our study is the first to describe clinical periodontal disease and the relative abundance of periodontal bacteria in these at-risk individuals. Our results support the hypothesis that local inflammation at mucosal surfaces, such as the gums in this case, may provide the primary trigger for the systemic autoimmunity seen in RA.”

The prevalence of gum disease is significantly higher in patients with RA, and could be a key initiator of RA-related autoimmunity. This is because autoimmunity in RA is characterised by an antibody response to citrullinated proteins, and the oral bacterium Porphyromonas gingivalis (Pg) is the only human pathogen known to express an enzyme that can generate citrullinated proteins.

In results from the study, dentists diagnosed clinical gum disease in significantly more at-risk individuals than in healthy controls (73% vs. 38%). In addition, the percentage of sites with clinical attachment level (CAL) 2mm, pocket depth (PD) 4mm, bleeding on probing (BOP), periodontal disease (PDD), and active periodontal disease (PDD+BOP), were all significantly greater in the at-risk individuals compared to controls (p<0.05). In non-smokers, PDD and active PDD were more prevalent in at-risk individuals compared to controls.

Bacterial DNA was isolated from subgingival plaque, next to the gums, of participants to identify and measure the presence of three types of bacteria, Porphyromonas gingivalis (Pg), Aggregatibacter actinomycetemcomitans (Aa) and Filifactor Alocis. Results showed that there was increased abundance of both Pg and Aa in at-risk individuals. However, in at-risk individuals, only Pg was significantly increased at healthy dental sites and was associated with the overall extent of gum disease (p<0.001).

The study included 48 at-risk individuals (positive test for anti-citrullinated protein antibodies, musculoskeletal symptoms but no clinical synovitis), 26 patients with RA and 32 healthy controls. The three groups were balanced for age, gender and smoking. At-risk individuals underwent ultrasound assessment to assess for subclinical synovitis; only two (4%) were found to have ultrasound synovitis. Dentists examined six sites per tooth in each participant and a clinical consensus was agreed in each by three dentists.

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